OBJECTIVE: To identify possible imbalance of tumour necrosis factor alpha (TNFalpha) and its soluble receptors in the different subgroups of juvenile chronic arthritis (JCA). METHODS: Serum and synovial fluid samples from 45 children were examined, 25 pauciarticular JCA, 13 polyarticular JCA and seven spondyloarthropathy. TNFalpha, sTNFRI and sTNFRII levels were measured by EASIA and enzyme-linked immunosorbent assay (ELISA). Analysis of the results was carried out using non-parametric tests: Kruskal-Wallis one-way analysis of variance was used to compare the three clinical subgroups; the Mann-Whitney U-test was used to compare group medians. RESULTS: Thirty-three serum samples were assayed for TNFalpha. There was no significant difference between the three groups using the Kruskal-Wallis analysis of variance. Analysis of synovial fluid TNF levels showed significantly lower levels in the spondyloarthropathy group compared with the pauciarticular JCA (P = 0.01) and the polyarticular group (P = 0.002). Significantly higher levels of sTNFRI were observed in the synovial fluid of the polyarticular JCA group compared with the pauciarticular JCA group (P = 0.004) and similarly for sTNFRII (P = 0.03). Molar ratios were calculated for TNF vs sTNFRI. The sTNFRI/TNFalpha ratio was significantly higher in the spondyloarthropathy group compared with the pauci- (P 0.003) and the polyarticular JCA subgroups (P = 0.003). The combined soluble receptor levels expressed as molar ratio to TNF again showed a significantly higher ratio in the spondyloarthropathy group compared with the pauciarticular group (P = 0.01) and compared with the polyarticular group (P = 0.05). CONCLUSION: These results suggest that the increased joint destruction observed in polyarticular disease compared with the other two subtypes may be related to the lower sTNFR/TNFalpha ratios observed.
OBJECTIVE: To identify possible imbalance of tumour necrosis factor alpha (TNFalpha) and its soluble receptors in the different subgroups of juvenile chronic arthritis (JCA). METHODS: Serum and synovial fluid samples from 45 children were examined, 25 pauciarticular JCA, 13 polyarticular JCA and seven spondyloarthropathy. TNFalpha, sTNFRI and sTNFRII levels were measured by EASIA and enzyme-linked immunosorbent assay (ELISA). Analysis of the results was carried out using non-parametric tests: Kruskal-Wallis one-way analysis of variance was used to compare the three clinical subgroups; the Mann-Whitney U-test was used to compare group medians. RESULTS: Thirty-three serum samples were assayed for TNFalpha. There was no significant difference between the three groups using the Kruskal-Wallis analysis of variance. Analysis of synovial fluid TNF levels showed significantly lower levels in the spondyloarthropathy group compared with the pauciarticular JCA (P = 0.01) and the polyarticular group (P = 0.002). Significantly higher levels of sTNFRI were observed in the synovial fluid of the polyarticular JCA group compared with the pauciarticular JCA group (P = 0.004) and similarly for sTNFRII (P = 0.03). Molar ratios were calculated for TNF vs sTNFRI. The sTNFRI/TNFalpha ratio was significantly higher in the spondyloarthropathy group compared with the pauci- (P 0.003) and the polyarticular JCA subgroups (P = 0.003). The combined soluble receptor levels expressed as molar ratio to TNF again showed a significantly higher ratio in the spondyloarthropathy group compared with the pauciarticular group (P = 0.01) and compared with the polyarticular group (P = 0.05). CONCLUSION: These results suggest that the increased joint destruction observed in polyarticular disease compared with the other two subtypes may be related to the lower sTNFR/TNFalpha ratios observed.
Authors: John R North; Shunsuke Takenaka; Annett Rozek; Agnieszka Kielczewska; Steven Opal; Lisa A Morici; B Brett Finlay; Christopher J Schaber; Richard Straube; Oreola Donini Journal: J Biotechnol Date: 2016-03-23 Impact factor: 3.307
Authors: H M Walters; N Pan; T J A Lehman; A Adams; G D Kalliolias; Y S Zhu; F Santiago; J Nguyen; L Sitaras; S Cunningham-Rundles; T J Walsh; S S Toussi Journal: Clin Exp Immunol Date: 2016-04-13 Impact factor: 4.330
Authors: C E Millett; J Harder; J J Locascio; M Shanahan; G Santone; R N Fichorova; A Corrigan; C Baecher-Allan; K E Burdick Journal: Brain Behav Immun Date: 2020-04-06 Impact factor: 7.217